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Vasoactive Continuous Infusions - Adult - Inpatient

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Vasoactive Continuous Infusions in Adult Patients – Adult – Inpatient
Clinical Practice Guideline
Table of Contents
A. Executive Summary .............................................................................................................................. 2
B. Scope .................................................................................................................................................... 4
C. Methodology .......................................................................................................................................... 4
D. Introduction ............................................................................................................................................ 4
E. Recommendations ................................................................................................................................ 5
F. UW Implementation ............................................................................................................................. 10
G. References .......................................................................................................................................... 12
CPG Contact:
Name: Philip Trapskin, PharmD, BCPS, Drug Policy Manager
Phone Number: 608-265-0341
Email address: PTrapskin@uwhealth.org
Guideline Author(s):
Updated by Melissa Heim, PharmD and Jeff Fish, PharmD
Anna Krupp, RN, MS
Cindy Gaston, PharmD
Coordinating Team Members:
A. Alexander, CNS, MS; S. Aton, PharmD; J. Fish, PharmD, S. Kraus, MS, RN; M. Murray, CNS,
MS; Critical Care Committee
Review Individuals/Bodies:
M. Heim, PharmD; C. Gaston, PharmD; J. Fish, PharmD; A. Krupp RN
Committee Approvals/Dates:
Critical Care Committee – August 2014
Original guideline approved by Pharmacy & Therapeutics Committee: May 2010
Revised guideline: October 2014
Release Date:
October 2014
Copyright © 2014 Univ ersity of Wisconsin Hospitals and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 10/2014CCKM@uwhealth.org

2
A. Executive Summary
Guideline Overview
The purpose of this guideline is to provide a framework for the ordering, initiation and titration of
specific vasoactive agents in critically ill adults
Practice Recommendations
1. General recommendations regarding vasopressors
1.1. Treat the underlying cause of cardiovascular instability, hypoxia and acidosis and fluid
resuscitate patients to response along with vasoactive agents 2,10 (Class I, Level A)
1.2. Consider a second vasopressor when one is not effective10,11 (Class I, Level B)
2. Norepinephrine
2.1. Use norepinephrine as the first line agent in the treatment of hypotension due to septic
shock10,12,13 (Class I, Level A)
2.2. Central line preferred, however, peripheral/intraosseous access may be used when benefit
outweighs risks14,15 (Class I, Level C)
3. Vasopressin
3.1. Add vasopressin to norepinephrine in patients with septic shock and insufficient response to
norepinephrine with the intent of raising mean arterial pressure to target or decreasing
norepinephrine dosage4,10 (Class I, Level A)
3.2. Central line preferred, however, peripheral/intraosseous access may be used when benefit
outweighs risks14,15 (Class I, Level C)
4. Epinephrine
4.1. Use epinephrine as the first line agent for patients with anaphylaxis16,17 (Class I, Level A)
4.2. Epinephrine may be added to or substituted for norepinephrine when blood pressure goals
are not attained in septic shock10 (Class 2b, Level B)
4.3. Central line preferred, however, peripheral/intraosseous access may be used when benefit
outweighs risks14,15 (Class I, Level C)
5. Dopamine
5.1. Use dopamine as an alternative vasopressor agent to norepinephrine for the treatment of
hypotension in patients with low risk of tachyarrhythmias and absolute or relative
bradycardia10,12,13 (Class I, Level A)
5.2. Do not use “renal dose” dopamine to preserve kidney function due to lack of evidence and
potential toxicity10,18,19 (Class III, Level A)
5.3. Central line preferred, however, peripheral/intraosseous access may be used when benefit
outweighs risks14,15 (Class I, Level C)
6. Phenylephrine
6.1. Do not use phenylephrine in the treatment of septic shock unless3,10 (Class 3, Level A)
6.1.1. norepinephrine is associated with serious arrhythmias
6.1.2. cardiac output is high and blood pressure is persistently low
6.1.3. used as salvage therapy when combined inotrope/vasopressor drugs and low-dose
vasopressin have failed to achieve mean arterial pressure target
6.2. Use phenylephrine as the recommended agent for treatment of hypotension in patients with
aortic stenosis, obstructive hypertrophic cardiomyopathy, or vagal induced hypotension
caused by phosphodiesterase inhibitors or nitrates2 (Class I, Level A)
6.3. Central line preferred, however, peripheral/intraosseous access may be used when benefit
outweighs risks14,15 (Class IIb, Level C)
7. General recommendations regarding inotropes
7.1. Until definitive therapy (e.g., coronary revascularization or heart transplantation) or resolution
of the acute precipitating problem, patients with cardiogenic shock should receive temporary
intravenous inotropic support to maintain systemic perfusion and preserve end-organ
performance5 (Class I, Level C)
7.2. Short-term, continuous intravenous inotropic support is useful in patients with severe systolic
dysfunction who present with low blood pressure and significantly depressed cardiac output
to maintain systemic perfusion and preserve end-organ performance5,20-22 (Class II, Level B)
Copyright © 2014 Univ ersity of Wisconsin Hospitals and Clinics Authority
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3
8. Dobutamine
8.1. For patients with septic shock, a trial of dobutamine infusion should be administered in the
presence of10,23 (Class I Level C)
8.1.1. Myocardial dysfunction (elevated cardiac filling pressures and low CO)
8.1.2. Ongoing signs of hypoperfusion despite achieving adequate intravascular volume and
adequate mean arterial pressure
8.2. For HF patients who have systolic dysfunction with low cardiac index and systemic
hypoperfusion and/or congestion refractory to fluid restriction, salt restriction, and diuretics,
dobutamine should be trialed to improve end-organ perfusion5,20-22 (Class II, Level B)
8.3. For patients with low CO associated with myocardial infarction, dobutamine should be
administered to improve cardiac output if no symptoms of shock are present6 (Class II, Level
B)
8.4. Central line preferred, however, peripheral/intraosseous access may be used when benefit
outweighs risks14,15 (Class I, Level C)
9. Milrinone
9.1. For HF patients who have systolic dysfunction with low cardiac index and systemic
hypoperfusion and/or congestion refractory to fluid restriction, salt restriction, and diuretics,
milrinone should be administered to improve end-organ perfusion5,20-22 (Class II, Level B)
9.2. Dose adjustment of milrinone is required for renal dysfunction (and is contraindicated in
patients receiving continuous renal replacement therapy) due risk of elevated milrinone
concentrations and life-threatening arrhythmias24-26 (Class I, Level B)
9.3. Use of milrinone should be limited in patients with myocardial ischemia21 (Class IIb, Level B)
10. General recommendations regarding vasodilators and antihypertensives
10.1. Treat hypertensive emergency with a continuous infusion of a short-acting, titratable
antihypertensive agent to avoid rapid reduction of BP7-9 (Class I, Level A)
10.2. In hypertensive emergency, the immediate goal is to reduce diastolic BP by 10 to 15% or
to approximately 110 mm Hg over a period of 30 to 60 minutes. If the patient is stable,
systolic BP can be further reduced to 160 mm Hg and DBP can be reduced to 100–110 mm
Hg over the ensuing 2–6 hours. A gradual reduction to the patient’s baseline “normal” BP is
targeted over the initial 24–48 hours if the patient is stable.7-9 (Class I, Level A)
11. Nitroprusside
11.1. Nitroprusside is a recommended vasodilator for patients with acute congestive heart
failure or acute pulmonary edema requiring rapid reduction in preload and afterload5,7-9
(Class I, Level A)
11.2. Do not use nitroprusside in patients with hypertension and acute myocardial infarction
due to increased risk of mortality7-9,27 (Class III, Level A)
11.3. Administration of nitroprusside with sodium thiosulfate is recommended to prevent
cyanide and thiocyanate toxicity, especially in patients with severe renal dysfunction7-9,28
(Class IIb, Level C)
11.4. Monitor for signs of cyanide and thiocyanate toxicity (metabolic acidosis, decreased
oxygen saturation, bradycardia, confusion, convulsions) if nitroprusside is used at doses
greater than 2 mcg/kg/min or for greater than three days7-9,28 (Class I, Level B)
12. Nitroglycerin
12.1. Nitroglycerin is used to reduce blood pressure in patients with acute congestive heart
failure, acute pulmonary edema, acute myocardial infarction, or perioperative hypertension5-9
(Class I, Level A)
12.2. Do not administer nitroglycerin within 24-48 hours of phosphodiesterase inhibitors, such
as sildenafil, tadalafil, or vardenafil.7-9 (Class III, Level A)
12.3. Nitroglycerin is not first line therapy for hypertensive urgencies due to side effects and
development of tolerance, but can be used as an adjunct agent. 7-9 (Class IIb, Level C)
13. Nicardipine
13.1. Use nicardipine for the treatment of hypertension associated with acute renal failure,
acute ischemic stroke/intracerebral bleed, eclampsia/pre-eclampsia, hypertensive
encephalopathy or sympathetic crisis/cocaine overdose.7-9,29 (Class I, Level A)
13.2. Do not use nicardipine in patients with advanced aortic stenosis.7-9,30-32 (Class III, Level
A)
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4
14. Diltiazem
14.1. Use diltiazem as a continuous IV infusion for rate control in supraventricular tachycardia
in patients without concomitant LV systolic dysfunction.33-35 (Class II, Level B)
14.2. Use diltiazem cautiously in treatment of patients with concomitant LV systolic dysfunction
because the negative inotropic effect can cause hypotension. (Class IIb, Level B)
15. Esmolol
15.1. Use esmolol to lower blood pressure in patients with severe post-operative hypertension
when there is increased CO, BP, and heart rate.7-9 (Class II, Level B)
15.2. Use caution when administering this drug to patients previously on β-blocker therapy or
with HF since these patients may be predisposed to bradycardia or precipitation of acute
heart failure. 7-9 (Class II, Level B)
15.3. Loading doses should be administered with initiation of infusion and rate increases due to
a very short duration of action. 7-9 (Class II, Level B)
16. Labetalol
16.1. Use labetalol continuous infusion for pregnancy-induced hypertensive crisis or
uncontrolled hypertension.7-9 (Class II, Level B)
16.2. Do not use labetalol in patients with reactive airway disease or chronic obstructive
pulmonary disease or in patients with second- or third- degree atrioventricular block or
bradycardia.7-9 (Class III, Level A)
16.3. Labetalol can be administered by multiple loading doses until desired BP is attained or as
a loading dose followed by a continuous infusion. 7-9 (Class II, Level B)
Companion Documents
Vasoactive Continuous Infusion Titration Protocol
Pertinent UW Health Policies & Procedures
Guideline for Non-chemotherapeutic agents: Prevention and Treatment of Chemical Phlebitis
and Extravasation of Peripherally Administered Non-chemotherapeutic Agents
High Alert Medication Administration
UWHC Guidelines for IV Administration of Formulary Medications in Adults
Patient Resources
None
B. Scope
The purpose of this guideline is to provide a framework for the ordering, initiation and titration of
specific vasoactive agents in critically ill adults
Target Population: Adult patients receiving vasoactive continuous infusions
C. Methodology
A modified Grading of Recommendations Assessment, Development and Evaluation (GRADE)
developed by the American Heart Association and American College of Cardiology has been
used to assess the Quality and Strength of the Evidence in this Clinical Practice Guideline
(Appendix 1).36
D. Introduction
Vasopressor, inotropic, vasodilatory and antihypertensive agents serve a vital role in supporting
the critical care patient and prompt titration of these agents is essential. Many vasoactive
medications are administered by continuous infusion with dose titration based on heart rate
(chronotropy), myocardial contractility (inotropy), and/or vascular resistance (vasoconstriction or
vasodilatation). The rate and frequency of dose titration is dependent upon the patient’s
individual hemodynamic parameters and response to therapy. Prompt titration is best
accomplished by the bedside nurse with continuous monitoring to parameters specified in
medication orders by the physician or other health care provider (Table 1, Table 2).
Copyright © 2014 Univ ersity of Wisconsin Hospitals and Clinics Authority
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5
E. Recommendations
1. General recommendations regarding vasopressors
1.1. Treat the underlying cause of cardiovascular instability, hypoxia and acidosis and fluid
resuscitate patients to response along with vasoactive agents 2,10 (Class I, Level A)
1.1.1. The etiology of shock can be sepsis, volume loss, brain and spinal cord injury,
anaphylaxis or a combination of factors. The first step in treatment is identification and
treatment of the underlying cause and fluid resuscitation.10 Without sufficient fluid
resuscitation, vasopressors are ineffective and can even be detrimental.1
1.2. Consider a second vasopressor when one is not effective10,11 (Class I, Level B)
1.2.1. Vasoactive medications such as dopamine, norepinephrine, epinephrine,
phenylephrine, and vasopressin are employed to treat circulatory shock, which is
generally defined as the inability to supply sufficient oxygen to tissues due to decreased
vascular perfusion. In general, vasopressors maintain tissue perfusion through an
increase in mean arterial pressure and cardiac output (CO). The preferred pressor for a
given patient must be determined by patient physiology, cause of shock and patient
response. When high doses of one vasoactive agent are insufficient to maintain blood
pressure (BP), then the addition of another vasopressor with a different mechanism of
action can improve BP response.10,11 These agents are standard treatment in intensive
care and emergency room settings but administration of vasopressors is not without
risks, which include induction or exacerbation of tachyarrhythmias and tissue necrosis.
2. Norepinephrine
2.1. Use norepinephrine as the first line agent in the treatment of hypotension due to septic
shock10,12,13 (Class I, Level A)
2.1.1. Norepinephrine is a first line vasopressor with potent α-receptor and moderate β1 and
β2 receptor agonist activity.1 It causes an increase in systolic, diastolic and pulse
pressures, but can increase or decrease CO depending upon SVR, ejection fraction
and reflex response. Norepinephrine is a first line agent in the treatment of hypotension
related to septic shock and preservation of tissue perfusion has been
demonstrated.10,12,13
2.2. Central line preferred, however, peripheral/intraosseous access may be used when benefit
outweighs risks14,15 (Class I, Level C)
2.2.1. Central line administration is preferred since extravasation results in tissue necrosis and
sloughing.14,15 (See Guideline for Non-chemotherapeutic agents: Prevention and
Treatment of Chemical Phlebitis and Extravasation of Peripherally Administered Non-
chemotherapeutic Agents) Extravasation should be treated immediately with
subcutaneous administration of diluted phentolamine, an α-receptor antagonist.14,15
Ischemia of the hepatic-splanchnic tissue with subsequent end organ damage is also
associated with norepinephrine administration.1,13
3. Vasopressin
3.1. Add vasopressin to norepinephrine in patients with septic shock and insufficient response to
norepinephrine with the intent of raising mean arterial pressure to target or decreasing
norepinephrine dosage4,10 (Class I, Level A)
3.2. Central line preferred, however, peripheral/intraosseous access may be used when benefit
outweighs risks14,15 (Class I, Level C)
3.2.1. Extravasation should be treated immediately with subcutaneous administration of
diluted phentolamine, an α-receptor antagonist.14,15
3.2.2. Vasopressin or “antidiuretic hormone” is released from the pituitary gland in response to
increased plasma osmolarity, hypotension, pain and hypoxia causing direct stimulation
of smooth muscle V1-receptors to cause peripheral vasoconstriction.1 During early
shock, a patient’s vasopressin concentration increases significantly, but as shock
progresses it declines to subnormal levels. Supplemental administration of vasopressin
via continuous infusion has been demonstrated to be effective in norepinephrine
resistant hypotension.10 The addition of low doses of vasopressin is recommended in
septic shock patients with an insufficient response to norepinephrine.4,10 Acidosis and
hypoxia have minimal impact on vasoconstriction mediated by vasopressin, unlike
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6
catecholamines. Doses greater than 0.04 units per minute are associated with coronary
vasoconstriction, peripheral necrosis, and splanchnic ischemia.
4. Epinephrine
4.1. Use epinephrine as the first line agent for patients with anaphylaxis16,17 (Class I, Level A)
4.2. Epinephrine may be added to or substituted for norepinephrine when blood pressure goals
are not attained in septic shock10 (Class 2b, Level B)
4.3. Central line preferred, however, peripheral/intraosseous access may be used when benefit
outweighs risks14,15 (Class I, Level C)
4.3.1. Extravasation should be treated immediately with subcutaneous administration of
diluted phentolamine, an α-receptor antagonist.14,15
4.3.2. Epinephrine is an alternative vasopressor with strong affinity for α, β1 and β2 receptors.
It also exhibits potent positive inotropic and chronotropic effects in addition to peripheral
vasoconstriction. Through direct pulmonary vasoconstriction and increased pulmonary
blood flow, arterial and venous pulmonary pressures are increased. Epinephrine is
recommended as an alternative agent for the treatment of septic shock in patients with
an inadequate response to norepinephrine.10 High doses can provoke dysrhythmias,
myocardial ischemia, and profound splanchnic vasoconstriction.3 Similar to
norepinephrine, epinephrine is preferably administered through a central line since
extravasation can cause severe tissue necrosis.14,15
5. Dopamine
5.1. Use dopamine as an alternative vasopressor agent to norepinephrine for the treatment of
hypotension in patients with low risk of tachyarrhythmias and absolute or relative
bradycardia10,12,13 (Class I, Level A)
5.1.1. Dopamine may cause more tachycardia and may be more arrhythmogenic than
norepinephrine.10,12,13
5.2. Do not use “renal dose” dopamine to preserve kidney function due to lack of evidence and
potential toxicity10,18,19 (Class III, Level A)
5.2.1. Dopamine also has a direct naturetic effect, and for years “renal dose” dopamine was
used in an effort to preserve kidney function, but this is no longer recommended due to
lack of evidence and potential toxicity.10,18,19
16.4. Central line preferred, however, peripheral/intraosseous access may be used when
benefit outweighs risks14,15 (Class I, Level C)
5.2.2. Extravasation of dopamine results in severe tissue necrosis and should be treated
immediately with subcutaneous administration of diluted phentolamine, an α-receptor
antagonist.14,15
5.2.3. Dopamine is an endogenous neurotransmitter that stimulates both the β and α-
receptors, causing vasoconstriction and raising both BP and heart rate (HR).1 It is an
immediate precursor to norepinephrine and exhibits a dose dependent physiological
effect. At low doses of 0.5 to 3 mcg/kg/min dopamine causes vasodilation in the
coronary, renal mesenteric and cerebral beds. This effect increases nearby blood flow,
but can result in tachycardia and hypotension in volume depleted patients.
Intermediate doses of dopamine (approximately 3 to 10 mcg/kg/min) promote
norepinephrine release and inhibit reuptake resulting in increased cardiac contractility
and chronotropy. Doses above 10 mcg/kg/min of dopamine cause the release of
norepinephrine from the nerve terminals resulting in vasoconstriction and an increase in
systemic vascular resistance (SVR). In patients the pharmacological effects of various
dose ranges overlaps.
6. Phenylephrine
6.1. Do not use phenylephrine in the treatment of septic shock unless3,10 (Class 3, Level A)
6.1.1. norepinephrine is associated with serious arrhythmias
6.1.2. cardiac output is high and blood pressure is persistently low
6.1.3. used as salvage therapy when combined inotrope/vasopressor drugs and low-dose
vasopressin have failed to achieve mean arterial pressure target
6.2. Use phenylephrine as the recommended agent for treatment of hypotension in patients with
aortic stenosis, obstructive hypertrophic cardiomyopathy, or vagal induced hypotension
caused by phosphodiesterase inhibitors or nitrates2 (Class I, Level A)
Copyright © 2014 Univ ersity of Wisconsin Hospitals and Clinics Authority
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7
6.3. Central line preferred, however, peripheral/intraosseous access may be used when benefit
outweighs risks14,15 (Class IIb, Level C)
6.3.1. Extravasation should be treated immediately with subcutaneous administration of
diluted phentolamine, an α-receptor antagonist.14,15
6.3.2. Phenylephrine exhibits potent α activity with virtually no β activity, resulting in venous
and arterial vasoconstriction. Hemodynamically this brings about an increase in SVR
with variable effects on CO. These properties are beneficial when treating hypotension
in patients with aortic stenosis, obstructive hypertrophic cardiomyopathy or vagal
induced hypotension caused by phosphodiesterase inhibitors or nitrates.2 By increasing
systolic, diastolic and mean arterial blood pressures, phenylephrine can cause reflex
bradycardia and is not indicated for use as a sole agent in the treatment of hypotension
associated with septic shock or anaphylaxis.3,10 Unlike other vasopressors, it can be
administered via rapid bolus for acute, severe hypotension or via a continuous infusion.
7. General recommendations regarding inotropes
7.1. Until definitive therapy (e.g., coronary revascularization or heart transplantation) or resolution
of the acute precipitating problem, patients with cardiogenic shock should receive temporary
intravenous inotropic support to maintain systemic perfusion and preserve end-organ
performance.5 (Class I, Level C)
7.2. Short-term, continuous intravenous inotropic support is useful in patients with severe systolic
dysfunction who present with low blood pressure and significantly depressed cardiac output
to maintain systemic perfusion and preserve end-organ performance5,20-22 (Class II, Level B)
7.2.1. Dobutamine and milrinone are the most commonly used inotropes for low output
cardiac conditions associated with increased ventricular filling pressure. The first line of
therapy for acute heart failure (HF) is fluid and salt restriction, followed by diuretics and
vasodilators.5 If response is insufficient and left ventricular filling pressure is elevated,
then inotropes can be considered for symptomatic relief and improved end organ
perfusion. Patients on these agents must be closely monitored for induction or
exacerbation of tachyarrhythmias and hypotension. A large retrospective trial
comparing dobutamine and milrinone in HF patients demonstrated no difference in
hospital mortality or hospital complications.37
8. Dobutamine
8.1. For patients with septic shock, a trial of dobutamine infusion should be administered in the
presence of10,23 (Class I Level C)
8.1.1. Myocardial dysfunction (elevated cardiac filling pressures and low CO)
8.1.2. Ongoing signs of hypoperfusion despite achieving adequate intravascular volume and
adequate mean arterial pressure
8.2. For HF patients who have systolic dysfunction with low cardiac index and systemic
hypoperfusion and/or congestion refractory to fluid restriction, salt restriction, and diuretics,
dobutamine should be trialed to improve end-organ perfusion5,20-22 (Class II, Level B)
8.3. For patients with low CO associated with myocardial infarction, dobutamine should be
administered to improve cardiac output if no symptoms of shock are present6 (Class II, Level
B)
8.4. Central line preferred, however, peripheral/intraosseous access may be used when benefit
outweighs risks14,15 (Class I, Level C)
8.4.1. Extravasation should be treated immediately with subcutaneous administration of
diluted phentolamine, an α-receptor antagonist.14,15
8.4.2. Dobutamine stimulates β1 and β2-receptors causing a chronotropic and strong inotropic
effect resulting in increased CO. At low doses it exhibits a mild vasodilatory effect and
BP can either decrease or increase when initiating therapy. Dobutamine is the first line
inotrope in septic patients with decreased CO with adequate BP.10 It is also
recommended to help improve HF symptoms and improve end-organ perfusion, but not
mortality, in patients with HF with systolic dysfunction and low cardiac index who are
refractory to other therapies and are suffering from end-organ hypoperfusion and/or
congestion.5,20-22 Tachyphylaxis has been documented after several days of treatment
and patients on β blockers can exhibit an attenuated response. The most common
adverse effects associated with the administration of dobutamine include an increase in
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8
myocardial oxygen consumption and exacerbation of ventricular arrhythmias.37 The
American College of Cardiology/American Heart Association Guidelines for the
Management of ST-Elevation Myocardial Infarction recommend dobutamine for low CO
associated with myocardial infarction if no symptoms of shock are present.6
9. Milrinone
9.1. For HF patients who have systolic dysfunction with low cardiac index and systemic
hypoperfusion and/or congestion refractory to fluid restriction, salt restriction, and diuretics,
milrinone should be administered to improve end-organ perfusion5,20-22 (Class II, Level B)
9.2. Dose adjustment of milrinone is required for renal dysfunction (and is contraindicated in
patients receiving continuous renal replacement therapy) due risk of elevated milrinone
concentrations and life-threatening arrhythmias24-26 (Class I, Level B)
9.3. Use of milrinone should be limited in patients with myocardial ischemia21 (Class IIb, Level B)
9.3.1. Similar to dobutamine, milrinone increases myocardial contractility and causes
peripheral vasodilation, resulting in improved hemodynamics in patients with acute HF
or low left ventricular output.5,20-22 It also decreases pulmonary vascular resistance and
SVR. Unlike dobutamine, it does not have β or chronotropic effects, but acts by
inhibiting the breakdown of intracellular cyclic adenosine monophosphate (cAMP) and
can be useful in patients with down-regulated adrenergic receptors such as HF patients.
Since the half-life is longer for milrinone than dobutamine, the time of onset and to
reach steady state is longer than dobutamine (Table 2). The longer half-life of milrinone
and renal elimination necessitate dose adjustment for renal dysfunction. 24-26 Milrinone
is contraindicated in patients receiving continuous renal replacement therapy.
Hypotension and dysrhythmias are the most common adverse events and some
clinicians omit a loading dose in an effort to minimize these events. Milrinone should be
avoided in patients with myocardial ischemia since it can increase morbidity and
mortality in this patient population.21
10. General recommendations regarding vasodilators and antihypertensives
10.1. Treat hypertensive emergency with a continuous infusion of a short-acting, titratable
antihypertensive agent to avoid rapid reduction of BP7-9 (Class I, Level A)
10.2. In hypertensive emergency, the immediate goal is to reduce diastolic BP by 10 to 15% or
to approximately 110 mm Hg over a period of 30 to 60 minutes. If the patient is stable,
systolic BP can be further reduced to 160 mm Hg and DBP can be reduced to 100–110 mm
Hg over the ensuing 2–6 hours. A gradual reduction to the patient’s baseline “normal” BP is
targeted over the initial 24–48 hours if the patient is stable.7-9 (Class I, Level A)
10.2.1. Continuous infusions of vasodilators also require close titration when used for the
treatment of HF or hypertensive emergencies and when BP must be decreased in a
controlled and predictable manner.5,7-9
10.2.2. Patient and drug specific characteristics direct selection of the appropriate agent
for treatment. Patients with a hypertensive emergency commonly exhibit symptoms of
headache, shortness of breath, epistaxis or severe anxiety and can suffer end organ
damage if BP is not controlled. Dangerous blood pressures can also be encountered
during cardiovascular surgery, neurosurgery, renal transplantation and trauma
surgery.7-9 Due to increased sympathetic tone and vascular resistance, the early post-
operative period can also be associated with high blood pressures. A controlled
decrease in blood pressure by titration of continuous infusions of short acting agents is
often the most appropriate method of treatment in these patients. Vasodilating agents
such as nitroglycerin, nitroprusside, and nicardipine are often used for hypertensive
treatment and improve preload and/or afterload.
11. Nitroprusside
11.1. Nitroprusside is a recommended vasodilator for patients with acute congestive heart
failure or acute pulmonary edema requiring rapid reduction in preload and afterload5,7-9
(Class I, Level A)
11.2. Do not use nitroprusside in patients with hypertension and acute myocardial infarction
due to increased risk of mortality7-9,27 (Class III, Level A)
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9
11.3. Administration of nitroprusside with sodium thiosulfate is recommended to prevent
cyanide and thiocyanate toxicity, especially in patients with severe renal dysfunction7-9,28
(Class IIb, Level C)
11.4. Monitor for signs of cyanide and thiocyanate toxicity (metabolic acidosis, decreased
oxygen saturation, bradycardia, confusion, convulsions) if nitroprusside is used at doses
greater than 2 mcg/kg/min or for greater than three days7-9,28 (Class I, Level B)
11.4.1. Cyanide is a byproduct of nitroprusside metabolism, which is hepatically
metabolized to thiocyanate. Thiosulfate is required for this conversion. Thiocyanate is
100 times less toxic than cyanide and is renally excreted. Cyanide can accumulate to
cause cyanide toxicity, particularly in patients with hepatic and/or renal insufficiency.
Patients with renal or hepatic dysfunction and on high doses of nitroprusside or
receiving treatment for more than three days are at risk for cyanide or thiocyanate
toxicity and must be monitored closely. Simultaneous administration of nitroprusside
and sodium thiosulfate can prevent cyanide toxicity by enhancing conversion to a less
toxic thiocyante.28
11.4.2. Nitroprusside acts on arteriolar and venous smooth muscle to reduce both
preload and afterload, making it useful in patients with acute congestive heart failure
and/or acute pulmonary edema. It causes a prompt reduction in BP and either an
increase or no change in CO. Unpredictable shifts in BP can occur if patients are
hypovolemic or exhibit diastolic dysfunction.7-9
12. Nitroglycerin
12.1. Nitroglycerin is used to reduce blood pressure in patients with acute congestive heart
failure, acute pulmonary edema, acute myocardial infarction, or perioperative hypertension5-9
(Class I, Level A)
12.2. Do not administer nitroglycerin within 24-48 hours of phosphodiesterase inhibitors, such
as sildenafil, tadalafil, or vardenafil7-9 (Class III, Level A)
12.2.1. Nitroglycerin dilates primarily the venous system to decrease preload, but high
doses also affect arterial smooth muscle. In volume-depleted patients, nitroglycerin
may cause reduced CO, reflex tachycardia, and reduced cerebral and renal perfusion.
It is recommended by the Heart Failure Society of American in the treatment of acute
HF in combination with salt and fluid restriction.5
12.2.2. The most common side effect of nitroglycerin administration is headache.
Methemogolbinemia is a rare side effect caused by prolonged nitroglycerin
administration.
12.3. Nitroglycerin is not first line therapy for hypertensive urgencies due to side effects and
development of tolerance, but can be used as an adjunct agent. (Class IIb, Level C)
13. Nicardipine
13.1. Use nicardipine for the treatment of hypertension associated with acute renal failure,
acute ischemic stroke/intracerebral bleed, eclampsia/pre-eclampsia, hypertensive
encephalopathy or sympathetic crisis/cocaine overdose7-9,29 (Class I, Level A)
13.2. Do not use nicardipine in patients with advanced aortic stenosis7-9,30-32 (Class III, Level A)
13.2.1. Nicardipine is a dihydropyridine calcium channel antagonist with high vascular
selectivity used for the treatment of hypertension associated with acute myocardial
ischemia, acute renal failure, acute ischemic stroke/intracerebral bleed, eclampsia/pre-
eclampsia, hypertensive encephalopathy and sympathetic crisis/cocaine overdose. 7-9,29
Although it acts as a cerebral vasodilator, it also decreases resistance in small
arterioles with a net effect of unchanged intracranial pressure. It demonstrates high
vascular selectivity with marked coronary and cerebral vasodilatory properties. Because
it exerts minimal effect on cardiac muscle or the sinoatrial node, patients demonstrate
minimal change in heart rate or myocardial contractility. The most common side effects
include: headache, hypotension, nausea and vomiting. 7-9,30-32
14. Diltiazem
14.1. Use diltiazem as a continuous IV infusion for rate control in supraventricular tachycardia
in patients without concomitant LV systolic dysfunction33-35 (Class II, Level B)
14.1.1. Diltiazem is a non-dihydropyridine calcium channel blocker which causes a
decrease in conductivity, myocardial contractility and peripheral vascular resistance. It
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10
is indicated for rate control for atrial arrhythmias, hypertension and during non-cardiac
surgery to reduce myocardial ischemia and supraventricular tachycardia.34,35 Parenteral
diltiazem is beneficial for rapid rate control, but not for cardioversion of atrial fibrillation
to normal sinus rhythm.33 Diltiazem is preferred over β-blockers for rate control in
patients with chronic obstructive pulmonary disease.
14.2. Use diltiazem cautiously in treatment of patients with concomitant LV systolic dysfunction
because the negative inotropic effect can cause hypotension. (Class IIb, Level B)
15. Esmolol
15.1. Use esmolol to lower blood pressure in patients with severe post-operative hypertension
when there is increased CO, BP, and heart rate7-9 (Class II, Level B)
15.1.1. Esmolol is a short-acting cardioselective β1-antagonist that decreases arterial
pressure by decreasing heart rate and myocardial contractility.7-9 It is also useful in the
treatment of patients with hypertensive crisis with acute myocardial ischemia, acute
aortic dissection, and peri-operative hypertension. Esmolol is eliminated via plasma
esterases and the antihypertensive effects of esmolol will resolve within 20 minutes of
discontinuation of infusion.
15.2. Use caution when administering this drug to patients previously on β-blocker therapy or
with HF since these patients may be predisposed to bradycardia or precipitation of acute
heart failure. 7-9 (Class II, Level B)
15.3. Loading doses should be administered with initiation of infusion and rate increases due to
a very short duration of action. 7-9 (Class II, Level B)
16. Labetalol
16.1. Use labetalol continuous infusion for pregnancy-induced hypertensive crisis or
uncontrolled hypertension7-9 (Class II, Level B)
16.2. Do not use labetalol in patients with reactive airway disease or chronic obstructive
pulmonary disease or in patients with second- or third- degree atrioventricular block or
bradycardia7-9 (Class III, Level A)
16.2.1. Labetalol is a combined selective α1 and nonselective β-antagonist that reduces
systemic vascular resistance and either maintains or minimally decreases HR7-9,29 The
α to β activity is 1:7 when given intravenously and allows for decreased SVR without a
decrease in total peripheral blood flow. Unlike esmolol, labetalol maintains CO and
reduces SVR without decreasing total peripheral, cerebral, renal or coronary blood flow.
The antihypertensive duration of labetalol will occur for 2-4 hours after drug
discontinuation.
16.3. Labetalol can be administered by multiple loading doses until desired BP is attained or as
a loading dose followed by a continuous infusion. 7-9 (Class II, Level B)
17. General recommendations for titration of vasoactive therapies1-9 (Class II, Level B)
17.1. The rate and frequency of dose titration is dependent upon the patient’s individual
hemodynamic parameters, patient’s response to therapy and clinical status, as assessed by
the nurse.
17.2. The lowest effective dose of the vasoactive agent ordered that achieves the stated
objective response is utilized.
17.3. Vasoactive infusions are weaned off as indicated in the titration columns of Table 1.
18. General recommendations for monitoring and documentation of vasoactive agents_ENREF_1
(Class II, Level B)
18.1. Vital signs are monitored and documented hourly and with each rate change, unless
patient requires active titration, and then the patient will have continuous monitoring and vital
signs and rate will be documented at least every 15 minutes.
18.2. An arterial line for continuous blood pressure monitoring is recommended for all patients
requiring dose titration per protocol.
F. UW Implementation
Benefits/Harms of Implementation
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11
Benefits of implementation include consistent dosing and use of vasoactive continuous infusions.
Harms of implementation include risk of extravasation.
Qualifying Statements
Many of the recommendations included in the guideline include recommendations from national
guidelines or expert opinion as much of the literature has studied impact of vasoactive
medications on symptoms and not on outcomes. The recommendations in this guideline may
change if more literature becomes available.
Implementation Tools/Plan –
1. Implemented in conjunction with the Vasoactive Continuous Infusion Titration Protocol
2. Administration of vasoactive agents
2.1. High alert medications require double-check (as specified in policy UWHC Policy 8.33)
and must be performed directly prior to administration, with each bag change, at shift
change, upon patient transfer, or when IV pump programming is outside of the
established IV pump decision support software limits (Alaris Guardrails®).
2.2. Upon initiation of each continuous vasoactive infusion, the compatibility of simultaneous
infusions will be verified by the RN and/or pharmacist.
2.3. Vasoactive continuous infusions will be infused using stopcock connectors, and will not
be “y-sited” into infusion ports on the IV tubing.
2.4. No continuous infusion vasoactive agents will be infused through CVP port, except when
no other lines or ports are available and a vasoactive infusion is required for emergency
administration. The amount of intermittent medication administration through the CVP
port should be limited to avoid bolus drug administration with bolus cardiac output
monitoring.
2.5. Continuous infusions of vasoactive medications through the PA port of the pulmonary
artery catheter can put patients at risk for pulmonary hypertension and must be
approved by the provider.
2.6. New IV tubing will be primed when there is a change in drug concentration.
2.7. All infusions will be administered as designated in the UWHC Guidelines for IV
Administration of Formulary Medications in Adults
3. Titration of vasoactive therapies
3.1. If the vasoactive agent reaches the “First Notification Value,” a prescribing provider
(identified as physician, advanced practice nurse prescriber or physician assistant) is
notified for consideration of additional treatments or alternate agent(s).
3.2. For agents without an absolute maximum dose, if the dose reaches the “Second
Notification Value”, the physician is notified for consideration of additional treatments or
alternate agent(s) before further titration of the current agent occurs.
3.3. If the dose of the vasoactive agent reaches the “Second Notification Value,” a physician
order is required to continue therapy at higher doses.
3.4. Providers enter nursing communication orders to initiate weaning of vasoactive
infusions.
3.5. When titrating multiple vasoactive agents, providers clarify the sequence of medication
titration through nursing communication orders (e.g., order of titration for weaning off for
multiple agents).
3.6. Initiation of weaning vasoactive medication(s) occurs after a provider enters a nursing
communication order for weaning of a specific agent with specific parameters (such as
mean arterial pressure or cardiac index).
4. Monitoring and documentation of vasoactive agents
4.1. The nurse will record each rate adjustment in the IV/IV MAR. If the patient requires
frequent titration, the patient will have continuous monitoring and the current rate will be
documented at least every 15 minutes.
4.2. Notes will be documented in the electronic medical record by the RN after each provider
notification for “First Notification Value” and the “Second Notification Value.”
Disclaimer
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12
This Clinical Practice Guideline provides an evidence-based approach for the use of vasoactive
agents. It is understood that occasionally patients will not match the conditions considered in the
guideline.
G. References
1. Mullner M, Urbanek B, Havel C, Losert H, Waechter F, Gamper G. Vasopressors for shock. Cochrane
Database Syst Rev. 2004(3):Cd003709.
2. Overgaard CB, Dzavik V. Inotropes and vasopressors: review of physiology and clinical use in
cardiovascular disease. Circulation. Sep 2 2008;118(10):1047-1056.
3. Ellender TJ, Skinner JC. The use of vasopressors and inotropes in the emergency medical treatment of
shock. Emerg Med Clin North Am. Aug 2008;26(3):759-786, ix.
4. Dunser MW, Mayr AJ, Ulmer H, et al. Arginine vasopressin in advanced vasodilatory shock: a prospective,
randomized, controlled study. Circulation. May 13 2003;107(18):2313-2319.
5. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a
report of the American College of Cardiology Foundation/American Heart Association Task Force on
Practice Guidelines. J Am Coll Cardiol. Oct 15 2013;62(16):e147-239.
6. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-
elevation myocardial infarction; A report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the
Management of patients with acute myocardial infarction). J Am Coll Cardiol. Aug 4 2004;44(3):E1-e211.
7. Marik PE, Varon J. Hypertensive crises: challenges and management. Chest. Jun 2007;131(6):1949-1962.
8. Rhoney D, Peacock WF. Intravenous therapy for hypertensive emergencies, part 2. Am J Health Syst
Pharm. Aug 15 2009;66(16):1448-1457.
9. Rhoney D, Peacock WF. Intravenous therapy for hypertensive emergencies, part 1. Am J Health Syst
Pharm. Aug 1 2009;66(15):1343-1352.
10. Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis Campaign: international guidelines for
management of severe sepsis and septic shock, 2012. Intensive Care Med. Feb 2013;39(2):165-228.
11. Egi M, Bellomo R, Langenberg C, et al. Selecting a vasopressor drug for vasoplegic shock after adult
cardiac surgery: a systematic literature review. Ann Thorac Surg. Feb 2007;83(2):715-723.
12. De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of
shock. N Engl J Med. Mar 4 2010;362(9):779-789.
13. Patel GP, Grahe JS, Sperry M, et al. Efficacy and safety of dopamine versus norepinephrine in the
management of septic shock. Shock. Apr 2010;33(4):375-380.
14. Cooper BE. High-dose phentolamine for extravasation of pressors. Clin Pharm. Oct 1989;8(10):689.
15. Hill JM. Phentolamine mesylate: the antidote for vasopressor extravasation. Crit Care Nurse. Nov-Dec
1991;11(10):58-61.
16. Lieberman P, Nicklas RA, Oppenheimer J, et al. The diagnosis and management of anaphylaxis practice
parameter: 2010 update. J Allergy Clin Immunol. Sep 2010;126(3):477-480.e471-442.
17. Sampson HA. Anaphylaxis and emergency treatment. Pediatrics. Jun 2003;111(6 Pt 3):1601-1608.
18. Bellomo R, Chapman M, Finfer S, Hickling K, Myburgh J. Low-dose dopamine in patients with early renal
dysfunction: a placebo-controlled randomised trial. Australian and New Zealand Intensive Care Society
(ANZICS) Clinical Trials Group. Lancet. Dec 23-30 2000;356(9248):2139-2143.
19. Holmes CL, Walley KR. Bad medicine: low-dose dopamine in the ICU. Chest. Apr 2003;123(4):1266-1275.
20. Abraham WT, Adams KF, Fonarow GC, et al. In-hospital mortality in patients with acute decompensated
heart failure requiring intravenous vasoactive medications: an analysis from the Acute Decompensated
Heart Failure National Registry (ADHERE). J Am Coll Cardiol. Jul 5 2005;46(1):57-64.
21. Cuffe MS, Califf RM, Adams KF, Jr., et al. Short-term intravenous milrinone for acute exacerbation of
chronic heart failure: a randomized controlled trial. Jama. Mar 27 2002;287(12):1541-1547.
22. Elkayam U, Tasissa G, Binanay C, et al. Use and impact of inotropes and vasodilator therapy in hospitalized
patients with severe heart failure. Am Heart J. Jan 2007;153(1):98-104.
23. Yealy DM, Kellum JA, Huang DT, et al. A randomized trial of protocol-based care for early septic shock. N
Engl J Med. May 1 2014;370(18):1683-1693.
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Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 10/2014CCKM@uwhealth.org

13
24. Cox ZL, Calcutt MW, Morrison TB, Akers WS, Davis MB, Lenihan DJ. Elevation of plasma milrinone
concentrations in stage D heart failure associated with renal dysfunction. J Cardiovasc Pharmacol Ther.
Sep 2013;18(5):433-438.
25. Hasei M, Uchiyama A, Iguchi N, et al. [A case of continuous infusion of milrinone during continuous
venovenous hemofiltration causing high plasma concentration of milrinone]. Masui. Feb 2005;54(2):180-
182.
26. Taniguchi T, Shibata K, Saito S, Matsumoto H, Okeie K. Pharmacokinetics of milrinone in patients with
congestive heart failure during continuous venovenous hemofiltration. Intensive Care Med. Aug
2000;26(8):1089-1093.
27. Cohn JN, Franciosa JA, Francis GS, et al. Effect of short-term infusion of sodium nitroprusside on mortality
rate in acute myocardial infarction complicated by left ventricular failure: results of a Veterans
Administration cooperative study. N Engl J Med. May 13 1982;306(19):1129-1135.
28. Hall VA, Guest JM. Sodium nitroprusside-induced cyanide intoxication and prevention with sodium
thiosulfate prophylaxis. Am J Crit Care. Sep 1992;1(2):19-25; quiz 26-17.
29. Varon J. Treatment of acute severe hypertension: current and newer agents. Drugs. 2008;68(3):283-297.
30. Curran MP, Robinson DM, Keating GM. Intravenous nicardipine: its use in the short-term treatment of
hypertension and various other indications. Drugs. 2006;66(13):1755-1782.
31. Silke B, Verma SP, Hussain M, et al. Comparative haemodynamic effects of nicardipine and verapamil in
coronary artery disease. Herz. Apr 1985;10(2):112-119.
32. Silke B, Verma SP, Hafizullah M, et al. Haemodynamic effects of nicardipine in acute myocardial infarction.
Postgrad Med J. 1984;60 Suppl 4:29-34.
33. Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients with
Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force
on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing
Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation):
developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.
Circulation. Aug 15 2006;114(7):e257-354.
34. Snow V, Weiss KB, LeFevre M, et al. Management of newly detected atrial fibrillation: a clinical practice
guideline from the American Academy of Family Physicians and the American College of Physicians. Ann
Intern Med. Dec 16 2003;139(12):1009-1017.
35. Kanji S, Stewart R, Fergusson DA, McIntyre L, Turgeon AF, Hebert PC. Treatment of new-onset atrial
fibrillation in noncardiac intensive care unit patients: a systematic review of randomized controlled trials.
Crit Care Med. May 2008;36(5):1620-1624.
36. Tricoci P, Allen JM, Kramer JM, Califf RM, Smith SC, Jr. Scientific evidence underlying the ACC/AHA clinical
practice guidelines. Jama. Feb 25 2009;301(8):831-841.
37. Yamani MH, Haji SA, Starling RC, et al. Comparison of dobutamine-based and milrinone-based therapy for
advanced decompensated congestive heart failure: Hemodynamic efficacy, clinical outcome, and
economic impact. Am Heart J. Dec 2001;142(6):998-1002.
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14
Appendix 1. Quality of Evidence and Strength of Recommendation Grading Matrix1
Copyright © 2014 Univ ersity of Wisconsin Hospitals and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 10/2014CCKM@uwhealth.org

15
Drug Typical Dose Range
Typical Starting
Dose
Dose Titration
Increment Rate of Titration
First Notification
Value
(notify provider
when dose is
reached)
Second
Notification Value
(notify provider
when dose is
reached)
Diltiazem 1-15 mg/hr 2.5-5 mg/hr 2.5 mg/hr 30-60 min 15 mg/hr 20 mg/hr
Dobutamine 2-20 mcg/kg/min 2 mcg/kg/min 2.5 mcg/kg/min 5-15 min 10 mcg/kg/min 15 mcg/kg/min
Dopamine 2-20 mcg/kg/min 2-5 mcg/kg/min 1-5 mcg/kg/min 1-15 min 15 mcg/kg/min 20 mcg/kg/min
Epinephrine 0.01 mcg/kg/min to
effect
0.01-0.05
mcg/kg/min
0.01-0.05
mcg/kg/min 1-15 min 0.4 mcg/kg/min 2 mcg/kg/min
Esmolol 50-300 mcg/kg/min 25-50 mcg/kg/min 50 mcg/kg/min 5-20 min 250 mcg/kg/min 300 mcg/kg/min
Labetalol 10-180 mg/hr 10 mg/hr 10 mg/hr 10-30 min 120 mg/hr 180 mg/hr
Milrinone 0.375-0.75 mcg/kg/min 0.375 mcg/kg/min 0.125 mcg/kg/min 15-30 min 0.5 mcg/kg/min 0.75 mcg/kg/min
Nicardipine 5-15 mg/hr 2.5-5 mg/hr 2.5 mg/hr 15-30 min 10 mg/hr 15 mg/hr
Nitroglycerin
(mcg/min) 5-200 mcg/min 5-10 mcg/min 5-20 mcg/min 5-15 min 200 mcg/min 300 mcg/min
Nitroglycerin
(mcg/kg/min) 0.2-3 mcg/kg/min 0.2 mcg/kg/min 0.2-0.5 mcg/kg/min 5-15 min 2 mcg/kg/min 3 mcg/kg/min
Nitroprusside 0.2-4 mcg/kg/min 0.2 mcg/kg/min 0.25-0.5 mcg/kg/min 1-15 min 4 mcg/kg/min 10 mcg/kg/min
Norepinephrine 0.01 mcg/kg/min to
effect
0.01-0.05
mcg/kg/min
0.01-0.05
mcg/kg/min 1-15 min 0.4 mcg/kg/min 2 mcg/kg/min
Phenylephrine 0.25 mcg/kg/min to
effect
0.25-0.5
mcg/kg/min 0.25 mcg/kg/min 1-15 min 3 mcg/kg/min 5 mcg/kg/min
Vasopressin
(septic shock)
0.01-0.04 units/min 0.04 units/min
Do not increase
rate without MD
Order. Wean off by
0.01 unit/min
30-60 min N/A N/A
Table 1. UWHC Guideline for Titration of Vasoactive Continuous Infusions1-9 Contact Drug Policy Program | Last revised: 10/2014
Vasoactive Continuous Infusion – Adult- Inpatient Guideline
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16

Drug Onset Duration T1/2 Primary Route of Elimination Noteworthy Adverse Effects/Comments
Diltiazem 3 min 1-3 hr 3-6.6 hr hepatic AV block, bradycardia, CHF exacerbation
Dobutamine 2 min 10 min 2 min hepatic Hypotension, dysrhythmias
Dopamine 5 min 10 min 2 min renal Tissue necrosis with extravasation,
dysrhythmias
Esmolol 1-2 min 10-30 min 9 min hydrolyzed by RBC esterases
Infusion site reactions, confusion,
bradycardia
Epinephrine 1-2 min 5-10 min 2 min hepatic Dysrhythmias, tissue necrosis, ischemia
Labetalol 5-15 min 2-4 hr 5.5 hr hepatic Hypotension, bradycardia
Milrinone 5-15 min 3-5 hr 1.5-2 hr renal
Hypotension, dysrhythmias, nausea,
vomiting. Clinical response may last up
to 24 hours in certain patients
Nicardipine 10 min 2 hr 2-4 hr hepatic Peripheral edema, tachyarrhythmia
Nitroglycerin 5-10 min 10-20 min 1-3 min hepatic Hypotension, reflex tachycardia if volume
depleted
Nitroprusside 1 min 1-2 hr 3-5 min hepatic Hypotension, cyanide/thiocyanate toxicity
Norepinephrine 1 min 15-30 min 5 min hepatic Dysrhythmias, tissue necrosis, ischemia
Phenylephrine 1 min 15-30min 15-30 min hepatic Extravasation causes tissue necrosis
Vasopressin
(septic shock)
5-15 min 30-60 min 10-20 min hepatic Dysrhythmias, tissue necrosis, ischemia
Table 2. Pharmacokinetic Parameters, Contraindications and Common Adverse Event 1-9
Contact Drug Policy Program | Last revised: 10/2014
Vasoactive Continuous Infusion – Adult- Inpatient
Guideline
Copyright © 2014 University of Wisconsin Hospitals and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 10/2014CCKM@uwhealth.org